The purpose of this study is to determine what happens to the number and distribution of sodium channels in regenerating, demyelinating and remyelinating nerve fibers and to correlate the changes with 1) changes in the conduction velocity and fatigability of the nerve fibers, 2) changes in the number of nodes of Ranvier, 3) changes in the staining properties of the nodal membrane undercoating, and 4) changes in the distribution of the 20 nm membrane particles seen on the external face of the nodal membrane in freeze fracture preparations. Results of this study should help to establish the postulated equivalence of the 20 nm membrane particles with the sodium channels. It should also allow us to determine the role played by changes in sodium channel number and distribution in recovery of conduction in demyelinated and remyelinating nerve fibers. Such a determination has important implications for human peripheral and central demyelinating diseases including Guillain Barre Syndrome and Multiple Sclerosis. A clearer understanding of the pathophysiology of conduction in the demyelinating diseases may lead to methods of improving nerve conduction and thus function in individuals with demyelinating diseases.